HSV-1 Remodels PI3-Kinase/AKT Signaling

• Author / Creator

  Quach, Kevin

• AKT inhibits apoptosis and stimulates cap-dependent translation by phosphorylating key downstream cellular proteins. Many viruses therefore activate the PI3-kinase-AKT signaling pathway to promote cell survival and viral protein synthesis. HSV-1 activates AKT during lytic infection and the abundant tegument protein VP11/12 is required for this effect. Although VP11/12 is essential for AKT activation, deleting VP11/12 has no detectable effect on HSV-1 induced phosphorylation of the examined downstream target proteins. Rather, the protein kinase US3 is required for the phosphorylation of AKT targets and thus serves as an AKT mimic. Our data indicate that VP11/12 and US3 do not collaborate to provide redundant coverage of key AKT targets during infection. Interestingly, HSV-1 attenuates signals from activated AKT induced by external growth factors. Remarkably, neither VP11/12 nor US3 is required for this effect.

• Subjects / Keywords

  • AKT
  • Us3
  • HSV-1
  • UL46
  • Herpes
  • VP11/12
  • PDGF
  • PI3K

• Graduation date

  Spring 2013

• Type of Item

  Thesis

• Degree

  Master of Science

• DOI

  https://doi.org/10.7939/R30S8T

• License

  This thesis is made available by the University of Alberta Libraries with permission of the copyright owner solely for non-commercial purposes. This thesis, or any portion thereof, may not otherwise be copied or reproduced without the written consent of the copyright owner, except to the extent permitted by Canadian copyright law.